Left ventricular hypertrabeculation/noncompaction (LVHT/NC) is associated with stroke or embolism (S/E). The aim of this retrospective study was to assess the rate, risk factors, and cause of S/E in patients with LVHT/NC. The medical records of patients with LVHT/NC were retrospectively screened for S/E. For stroke classification, the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria were applied, and for peripheral embolism, angiographic findings were used. Baseline clinical, echocardiographic, and electrocardiographic data were compared between patients with and without S/E. In 22 of 144 patients (15%), stroke (n = 21) or peripheral embolism (n = 1) had occurred. The cause of S/E was cardioembolic (n = 14), atherosclerotic (n = 5), or undetermined (n = 3). S/E occurred before (n = 14) and after (n = 8) the diagnosis of LVHT/NC. Only mean age (60 vs 53 years, p <0.05) and the prevalence of hypertension (32% vs 59%, p <0.05) were higher in patients with S/E than in those without S/E. Among patients with cardioembolic S/E, 13 of 14 had either atrial fibrillation (AF) or systolic dysfunction, and AF as well as systolic dysfunction were found in 4 of 14 patients. In conclusion, S/E in patients with LVHT/NC is not always cardioembolic but may also have an atherosclerotic cause. In the absence of AF or left ventricular systolic dysfunction, cardioembolic S/E is rare in patients with LVHT/NC. These findings suggest that patients with LVHT/NC with systolic dysfunction or AF should receive oral anticoagulation as primary prophylaxis against S/E.
Left ventricular hypertrabeculation/noncompaction (LVHT/NC) is a cardiac abnormality of unknown origin associated with heart failure, arrhythmias, and stroke or embolism (S/E). LVHT/NC is frequently associated with neuromuscular disorders. It is controversial if LVHT/NC per se favors S/E or if S/E occurs mainly if associated with systolic dysfunction or atrial fibrillation (AF). The aim of the retrospective study was to assess the rate, risk factors, and cause of S/E in patients with LVHT/NC.
Methods
Included were consecutive patients in whom LVHT/NC was diagnosed in the echocardiography laboratory of Krankenanstalt Rudolfstiftung (Vienna, Austria) from June 1995 to May 2009. Two-dimensional and Doppler echocardiographic criteria for the diagnosis of LVHT/NC were >3 trabeculations protruding from the left ventricular wall, apically to the papillary muscles, visible in 1 echocardiographic image plane; intertrabecular spaces perfused from the ventricular cavity, as visualized on color Doppler imaging; and a double-layered structure of the myocardium, consisting of a trabeculated and a nontrabeculated layer, best visualized at end-systole. The diagnostic criteria remained the same during the study period. The echocardiographic equipment were an Aloka 870 (Aloka, Wallingford, Connecticut; June 1995 to April 1998), a Vingmed System Five (GE Vingmed Ultrasound AS, Horten, Norway; May 1998 to December 2004), and a Vivid 7 (GE Healthcare, Milwaukee, Wisconsin; from January 2005) with 2.5- to 3.6-MHz transducers. The examinations were carried out by C.S. or G.B. and jointly reviewed by C.S. and G.B. Since planimetry was not feasible because of the trabeculations, systolic function was assessed by measuring left ventricular fractional shortening. Systolic dysfunction was diagnosed in patients with left ventricular fractional shortening <25%.
All patients underwent baseline examinations during which they were asked for their medical histories and cardiovascular symptoms and duration. Hypertension was diagnosed if a patient had a history of arterial hypertension and received ≥1 antihypertensive drug. A clinical examination was carried out, and 12-lead electrocardiography was registered. All patients were invited for neurologic investigations comprising histories and clinical neurologic examinations. If there were indications of polyneuropathy, an established screening program for polyneuropathy, including blood tests, cerebrospinal fluid investigation, and nerve biopsy, was carried out. If there were indications of myopathy, a screening for myopathy was initiated, including muscle enzymes, electromyography, and occasionally muscle biopsy. Baseline data and findings were stored.
From January and March 2010, the records of all LVHT/NC patients available in the computer information system comprising all community hospitals in Vienna were screened if S/E had ever occurred before or after the diagnosis of LVHT/NC. For classification of stroke cause, the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria were applied, and for peripheral embolism, angiographic findings were used. Baseline clinical, echocardiographic, and electrocardiographic data and results of neurologic investigations were compared between patients with and without S/E. Group comparisons for noncategorical data were carried out using Student’s t tests. Categorical data were analyzed using chi-square tests and 2-sided Fisher’s exact tests.
Results
From June 1995 to May 2009, 46,793 patients underwent transthoracic echocardiography in the echocardiographic laboratory of the Krankenanstalt Rudolfstiftung. LVHT/NC was diagnosed in 144 patients (0.03%). Cerebrovascular events and follow-up data of a subgroup of these patients have been published. In 22 of 144 patients (15%), ≥1 stroke (n = 21) or peripheral embolism (n = 1) occurred. The cause of S/E was cardioembolic (n = 14), atherosclerotic (n = 5), or undetermined (n = 3). S/E occurred either before (n = 14) or after (n = 8) the diagnosis of LVHT/NC. At the time of S/E, 13 patients received acetylsalicylic acid 100 mg/day, 1 patient was receiving oral anticoagulation with an international normalized ratio below the therapeutic range, 1 patient was taking low–molecular weight heparin, and 7 patients had no antithrombotic therapy at all. Only age and the prevalence of hypertension were higher in patients with S/E than in patients without ( Table 1 ). Neuromuscular disorders of unknown origin (79 vs 44%), AF (43 vs 15%), and LVHT/NC affecting the posterior wall (36 vs 14%) were more frequent in the 14 patients with cardioembolic stroke than in the remaining 130 patients (p <0.05). The 14 patients with cardioembolic S/E more frequently had heart failure (79% vs 13%, p <0.01), advanced stages of heart failure (57% vs 0%, p <0.01), and less frequently no electrocardiographic abnormalities (0% vs 38%, p <0.05) than the 8 patients with noncardioembolic causes.
| Characteristic | Total (n = 144) | S/E | |
|---|---|---|---|
| Yes (n = 22) | No (n = 122) | ||
| Age (years) | 54 ± 16.14 | 60 ± 15.15 | 53 ± 16.15 ⁎ |
| Women | 43 (30%) | 9 (41%) | 37 (28%) |
| Neurologically normal | 16 (11%) | 1 (5%) | 15 (12%) |
| Specific neuromuscular disorder | 22 (15%) | 2 (9%) | 20 (16%) |
| Neuromuscular disorder of unknown cause | 68 (47%) | 14 (64%) | 54 (44%) |
| Neurologically not investigated | 38 (26%) | 5 (23%) | 33 (27%) |
| Exertional dyspnea | 95 (66%) | 14 (64%) | 81 (66%) |
| Diabetes mellitus | 25 (17%) | 6 (27%) | 19 (16%) |
| Arterial hypertension | 52 (36%) | 13 (59%) | 39 (32%) ⁎ |
| Heart failure | 98 (68%) | 12 (55%) | 86 (71%) |
| Coronary heart disease | 13 (9%) | 1 (5%) | 12 (10%) |
| NYHA class I or II | 33 (23%) | 4 (36%) | 29 (24%) |
| NYHA class III or IV | 65 (45%) | 8 (36%) | 57 (47%) |
| No ECG abnormality | 15 (10%) | 3 (14%) | 12 (10%) |
| Left bundle branch block | 26 (18%) | 4 (18%) | 22 (18%) |
| Pathologic Q waves | 14 (10%) | 4 (18%) | 10 (8%) |
| AF | 25 (17%) | 6 (27%) | 19 (16%) |
| Left ventricular end-diastolic diameter >57 mm | 89 (62%) | 14 (64%) | 75 (62%) |
| Left ventricular fractional shortening <25% | 88 (61%) | 14 (64%) | 74 (61%) |
| LVHT/NC location | |||
| Apex | 135 (94%) | 21 (96%) | 114 (93%) |
| Anterior wall | 5 (3%) | 1 (5%) | 4 (3%) |
| Posterior wall | 23 (16%) | 6 (27%) | 17 (14%) |
| Lateral wall | 66 (46%) | 13 (60%) | 53 (43%) |
| Septal wall | 1 (1%) | 0 (0%) | 1 (1%) |
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
